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PubMed1986

Interaction of vitamin C and selenium supplementation in the modification of mammary carcinogenesis in rats.

The objectives of this study were a) to compare the efficacy of inorganic and organic selenium compounds in protecting against mammary tumorigenesis induced by 7,12-dimethylbenz[a]anthracene [(DMBA); CAS: 57-97-6] in rats and b) to study the interaction of vitamin C with either selenite (inorganic) or seleno-DL-methionine (organic) in chemoprevention. Control Sprague-Dawley rats were fed a purified 5% corn oil diet containing 0.1 ppm selenium. Selenite or seleno-DL-methionine was added to the basal diet in concentrations of 2, 3, or 4 ppm starting 1 week after DMBA administration. The inhibitory response in mammary tumorigenesis with selenium supplementation was dose dependent. Both selenium compounds were found to be equally efficacious in prophylaxis, although at the 4-ppm level a slight reduction in growth was observed. In the second experiment, different concentrations of vitamin C (0.2, 0.5, and 1%) were tested. In general, there was no change with the two lower levels; but a slight, although insignificant, increase in tumor yield was detected in rats supplemented with 1% vitamin C in the diet. The interaction of 0.5% vitamin C with either selenite or seleno-DL-methionine (3 ppm) was studied in the third experiment. Results showed that the protective effect of selenite in tumorigenesis was nullified by vitamin C, whereas the chemopreventive action of seleno-DL-methionine was not affected. It is possible that selenite is reduced by vitamin C to elemental selenium and is therefore not available for uptake by tissues. This hypothesis was indirectly supported by tissue selenium measurements showing that 0.5 or 0.25% of vitamin C in the diet completely negated in blood, liver, and mammary gland the accumulation of selenium induced by 3 ppm of selenite supplementation. Lower levels of vitamin C (less than or equal to 0.1%) were found to have no effect on tissue selenium concentrations. Furthermore, the presence of 0.1% vitamin C in the diet no longer abolished the anticarcinogenic effect of selenite. This study suggests that high levels of vitamin C can interfere with the accumulation of tissue selenium and that an increased titer of this trace element in cells is essential for retarding tumor development.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2006

Arsenic and selenium capture by fly ashes at low temperature.

Arsenic and selenium compounds may be emitted to the environment during coal conversion processes, although some compounds are retained in the fly ashes, in different proportions depending on the characteristics of the ashes and process conditions. The possibility of optimizing the conditions to achieve better trace element retention appears to be an attractive, economical option for reducing toxic emissions. This approach requires a good knowledge of fly ash characteristics and a thorough understanding of the capture mechanism involved in the retention. In this work the ability of two fly ashes, one produced in pulverized coal combustion and the other in fluidized bed combustion, to retain arsenic and selenium compounds from the gas phase in coal combustion and coal gasification atmospheres was investigated. To explore the possible simultaneous retention of mercury, the influence of the unburned coal particle content was also evaluated. Retention capacities between 2 and 22 mg g(-1) were obtained under different conditions. The unburned coal particle content in the fly ash samples does not significantly modify retention capacities.

Air Pollution↗
PubMed1996

Selenium status in infants and children with phenylketonuria and in maternal phenylketonuria.

The selenium status was investigated in 87 patients of the German Collaborative Study of Phenylketonuria (PKU) (mean age 9.7 years). The selenium values and glutathione peroxidase activity in plasma and erythrocytes were negatively correlated to the quality of dietary management (mean plasma phenylalanine value). Despite a low selenium state, the children showed no clinical sign of deficiency and almost all biochemical parameters checked were normal. In the low selenium state thyroxine values are increased and decline during selenium supplementation, whereas tri-iodothyronine and thyroid stimulating hormone levels remain unchanged. The reduction in glutathione peroxidase activity in plasma was more pronounced than in the erythrocytes pointing to a different availability of both enzymes for selenium. In addition we estimated the selenium status in 29 women with PKU during pregnancy. In 32 healthy pregnant women we observed a decrease in plasma selenium values and the glutathione peroxidase activity in the third trimester, whereas the erythrocyte glutathione peroxidase activity remained stable. In contrast to the healthy women we found in the PKU group a steady decrease of all selenium parameters tested during the whole pregnancy. During the long-term low-dose selenium supplementation in PKU children the glutathione peroxidase activity of plasma and erythrocytes increased. They reached a similar plateau after the application of inorganic or organic selenium compounds. In contrast the selenium values of plasma and whole blood showed only a plateau after the application of sodium selenite. The supplementation with low doses of selenium in the form of selenomethionine increased the plasma and whole blood selenium values constantly within the first 9 months. Therefore selenomethionine supplementation cannot be recommended.

Child↗
PubMed1997

[Inhibiton of endogenous synthesis of nitroso compounds by Selenium in rats].

The inhibiting effect of organic Se (selen-enriched yeast Bioselen) on the endogenous synthesis of N-nitrosubstances was investigated in the Wistar rats, receiving 15 mg of sodium nitritis and 24 mg of diethylamin per 1 kg of bodyweight during 22 days. The level of nitrosoprolin synthesis and (NPro) and the level of nitrosodiethyl (NDie) in the stomach of rats served as the main indices. The highest level of NPro and NDie were revealed in the rats, without selen supplementation (581.2 +/- 113.3 mg per kg of bodyweight and 29.8 +/- 3.0 mg per kg of bodyweight). The highest inhibiting effect of Se was 54.5% for NPro and 54.7% for NDie and it was shown for the Se concentration of 1.5 mg per 1 kg of forage. The increase of Se dosage to 3.0 mg per 1 kg of forage was less effective and resulted in 25.5% of inhibiting of NPro u 47.0% - NDie.

Administration, Oral↗
PubMed1990

Selective reduction of cis-diamminedichloroplatinum(II) nephrotoxicity by ebselen.

2-Phenyl-1,2-benzisoselenazol-3(2H)-one (ebselen) is classified as a relatively nontoxic selenium compound, probably because of its bound selenium moiety. In thiol-rich tissues, such as the kidneys, ebselen is converted into selenol intermediates. Selenols are nucleophilic agents which might be able to react with platinum compounds. The influence of ebselen on cis-diamminedichloroplatinum(II) (cisplatin)-induced nephrotoxicity in mice was assessed, using single doses of both compounds. Ebselen prevented cisplatin-induced elevations of blood urea nitrogen and serum creatinine levels and morphological kidney damage in BALB/c mice. This protective effect of ebselen was dose dependent: at a cisplatin dose of 14.5 mg/kg, maximal protection was achieved when a single dose of 10 mg of ebselen/kg was administered 1 h before cisplatin. Administration of ebselen, 10 mg/kg, 1 h after cisplatin also protected against severe nephrotoxicity. Treatment with ebselen did not reduce the antitumor activity of cisplatin against MPC 11 plasmacytoma or Prima breast tumor in BALB/c mice. However, this reduction of cisplatin-induced nephrotoxicity would be of little clinical value if it was achieved at toxic doses of ebselen. Ebselen, 10 mg/kg, did not induce blood urea nitrogen, serum creatinine, serum glutamic pyruvate transaminase, or serum glutamic oxalate elevations in the mice. These results are in agreement with the reported low toxicity of ebselen, which is now in Phase I clinical trials as an antiinflammatory drug. The present results indicate that ebselen may provide protection against cisplatin-induced nephrotoxicity, when it is given before or after cisplatin. This might open new perspectives in cancer chemotherapy.

Animals↗
PubMed1993

Homocysteine-dependent demethylation of trimethylselenonium ion and selenobetaine with methionine formation.

In the presence of rat liver cytosol and homocysteine, trimethylselenonium ion (TMSe+) underwent time-dependent demethylation to dimethylselenide with the concurrent formation of methionine. Convenient methods were developed for assay of this activity using either radioactive methods based on the gamma emitting isotope 75Se or nonradioactive HPLC assay of methionine. The rate of demethylation was linear with protein concentration and dependent on homocysteine, which could not be replaced by cysteine, glutathione, or dithiothreitol. The TMSe+ demethylation rate was inhibited by the addition of betaine, sulfobetaine (dimethylthetin), or dimethylglycine. The Km for TMSe+ was 8 mM compared to 0.04 mM for betaine, but the rate of TMSe+ demethylation was approximately 50-fold that of betaine when both were assayed at 25 mM. Methionine was also produced from selenobetaine, selenobetaine methylester, and sulfobetaine. The selenium analogues of betaine inhibited the demethylation of TMSe+ with only minor decreases in methionine production, indicating substrate competition. In preliminary studies aimed at the partial purification of the TMSe+:homocysteine methyltransferase activity, the enzyme was found to have chromatographic and heat stability characteristics similar to betaine:homocysteine methyltransferase. The data indicate that betaine:homocysteine methyltransferase, or a very similar enzyme, is involved in the demethylation of TMSe+ and show that TMSe+, an in vivo urinary selenium metabolite of many selenium compounds, is not biologically inert.

Animals↗
PubMed1999

Determination of dialkyldiselenides in water by gas chromatography-mass spectrometry using 1-fluoro-2,4-dinitrobenzene as derivatization reagent.

The feasibility of gas chromatography-mass spectrometry for the speciation of traces of dialkyldiselenides in the presence of dialkylselenides and inorganic selenium species is described, and the procedure is applied to environmental samples. The analysis is based on the reaction of dialkyldiselenide species with 1-fluoro-2,4-dinitrobenzene after volatilization of selenium species as alkylselenols using a volatilization and trap device. Parameters affecting the volatilization and derivatization of the selenium compounds are discussed, and the performance of the method is described. The approach reaches detection limits in the order of nanograms (after a preconcentration step) and has been applied to the analysis of dimethyldiselenium and diethyldiselenium in natural waters.

Dinitrofluorobenzene↗
PubMed2001

Thioredoxin reductase activity in rat liver is not affected by supranutritional levels of monomethylated selenium in vivo and is inhibited only by high levels of selenium in vitro.

Thioredoxin reductase is a selenoenzyme responsible for maintaining thioredoxin in the reduced form. Because thioredoxin is involved in many cellular processes, thioredoxin reductase is likely to be an important regulatory protein for both normal and transformed cells. Monomethylated selenium compounds inhibit carcinogenesis. In the present study, we investigated whether methylated forms of selenium would alter thioredoxin reductase activity in rats. The liver enzyme was used as a model system. Se-methylselenocysteine and methylseleninic acid consumed by rats at 2 microg Se/g diet for 3, 6, 10 or 22 wk did not affect activity compared with a basal diet containing 0.1 microg Se/g. The direct addition of 50 micromol dimethyl diselenide or dimethyl selenenylsulfide per L to liver extracts significantly inhibited thioredoxin reductase activity by approximately 60%. The magnitude of inhibition was dependent on the amount of thioredoxin in the assay and was reversible by dialysis, suggesting that a competitive type of inhibition occurs in vitro. Although thioredoxin reductase can be inhibited by high levels of selenium in a cell-free system, it should be noted that such a condition is unlikely to be attainable in vivo. Caution needs to be exercised in interpreting the in vitro results.

Animals↗
PubMed2000

Ebselen: prospective therapy for cerebral ischaemia.

Stroke occurs due to haemorrhage or occlusive injury and results in ischaemia and reperfusion injury. A variety of destructive mechanisms are involved including oxygen radical generation, calcium overload, cytotoxicity and apoptosis as well as the generation of inflammatory mediators. Ebselen, 2-phenyl-1, 2-benzisoselenazol-3(2H)-one (PZ 51, DR3305), is a mimic of GSH peroxidase which also reacts with peroxynitrite and can inhibit enzymes such as lipoxygenases, NO synthases, NADPH oxidase, protein kinase C and H(+)/K(+)-ATPase. Ebselen is in a late stage of development for the treatment of stroke. The molecular actions of ebselen contribute to its anti-inflammatory and anti-oxidant properties, which have been demonstrated in a variety of in vivo models. Numerous in vitro experiments using isolated LDL, liposomes, microsomes, isolated cells and organs have established that ebselen protects against oxidative challenge. Unlike many inorganic and aliphatic selenium compounds, ebselen has low toxicity as metabolism of the compound does not liberate the selenium moiety, which remains within the ring structure. Subsequent metabolism involves methylation, glucuronidation and hydroxylation. Experimental studies in rats and dogs have revealed that ebselen is able to inhibit both vasospasm and tissue damage in stroke models, which correlates with its inhibitory effects on oxidative processes. Results from randomised, placebo-controlled, double-blind clinical studies on the neurological consequences of acute ischaemic stroke, subarachnoid haemorrhage and acute middle cerebral artery occlusion, have revealed that ebselen significantly enhances outcome in patients who have experienced occlusive cerebral ischaemia of limited duration. The benefit achieved with ebselen is closely related to the rapidity with which the treatment is initiated, following the onset of the stroke attack. Safety and tolerability are good and no adverse effects have become apparent. Ebselen is currently at the pre-registration stage for subarachnoid haemorrhage and stroke in Japan.

Animals↗
PubMed1987

Comparison of the protection given by selenite, selenomethionine and biological selenium against the renotoxicity of mercury.

The protective effect of selenite, seleno-dl-methionine and biological selenium against the renotoxicity of mercury was tested in rats. As the source of biological selenium, the liver soluble fraction of rats given 60 mumoles/kg selenite 3 days before sacrifice was used. The aim of the experiments was to test whether protective efficiency follows the reported order of ability to form HgSe. Mercury was given subcutaneously in doses of 2.5, 5.0 and 7.5 mumoles/kg HgCl2 and selenium was given in equimolar doses at the same time as Hg2+. Liver soluble fraction, biological selenium or liver soluble fraction supplemented with selenite or seleno-dl-methionine were given orally, while in experiments without liver soluble fraction the two selenium compounds were given subcutaneously. Biological selenium was tested only at the two lower dose levels. Both biological selenium and seleno-dl-methionine decreased the urinary excretion of mercury in the first 48 h, but less so than selenite and only selenite decreased the renal content of mercury at the end of this period. Urinary alkaline phosphatase activity and plasma urea nitrogen at the 2.5 and 5.0 mumoles/kg dose levels decreased in the order of no selenium greater than biological selenium greater than seleno-dl-methionine greater than selenite. As the reported HgSe formation increases in the same order, the experiments support the role of HgSe formation in the protective effect. The degree of necrotic damage in the P2 and P3 regions of the proximal tubular cells increased in the same order as the biochemical indicators at the 5.0 and 7.5 mumoles/kg dose levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1975

X-ray photoelectron spectroscopy of some selenium containing amino acids.

X-ray photoelectron spectra of some inorganic selenium compounds, Se-methionine, Se-cystine, Se-urea and selenodicysteine were recorded and compared with the XPS data obtained from the respective sulphur containing compounds. The oxidation state of selenium could be monitored by the observed chemical shifts of the Se(3p1/2),Se(3p3/2) and Se(3d3/2,5/2) levels. Though having a formal oxidation state near zero, the binding energy of the core electrons of Se in Se-methionine, Se-cystine and selenodicysteine was shifted by 0.4, 0.7 and 0.4 eV, respectively. This phenomenon was attributed to the rather distinct polarization of Se. The reversible oxidation of Se-cystine using H2O2 and NaBH4 could be successfully demonstrated by this XPS-technique.

Amino Acids↗
PubMed1975

Modification of a selenium toxicity in chicks by dietary silver and copper.

Studies were conducted to determine the effects of high levels of dietary silver nitrate and copper sulfate on the response of chicks to toxic levels of dietary selenium. Adding 5 ppm or more selenium to a basal stock diet significantly reduced growth rate, and 40 ppm or high significantly increased mortality during the 2-week experiments. Deitary silver or copper (1,000 ppm) counteracted the growth depression and prevented mortality at the higher levels of selenium. Hepatic selenium reached a maxiumum in chicks fed the basal diet with 10 ppm dietary selenium. Hepatic selenium of chicks fed silver was less than that of the control chicks when diets containing 10 ppm or less selenium were fed. Adding copper to the diet resulted in considerable accumulation of selenium in the liver, which was evident even at the lower levels of added selenium. Rseults of an experiment to determine the effects of deitray silver and copper on the distribution of 75-Se administered either orally or in tramusculary showed that silver interfered with absorption of selenium. The results of these experiments suggest that silver modifies selenium toxity both by interfering with selenium absorption and by causing the accumulation of a nondeleterious selenium compound in the tissues. Copper modifies selenium toxicity primarily by causing the accumulation of a nondeleterious compound in the tissues.

Administration, Oral↗
PubMed1986

The metabolism of selenomethionine, Se-methylselenocysteine, their selenonium derivatives, and trimethylselenonium in the rat.

The formation of dimethylselenide (respiratory) and trimethylselenonium (urinary) metabolites from [75Se]selenomethionine, [75Se]methylselenomethionineselenonium, [75Se]methylselenocysteine, [75Se]dimethylselenocysteineselenonium, and [75Se]trimethylselenonium was determined using single sc doses of 2 or 0.064 mg Se/kg in male and female rats. The 75Se content of liver, kidney, pancreas, testis, spleen, blood, heart, brain, and skeletal muscle was determined at 0.5 and 24 h. Respiratory 75Se after 24 h was greatest from Se-dimethylselenocysteineselenonium (38 and 17% for the high and low doses, respectively). Respiratory 75Se was about 8% for the high dose of Se-methylselenocysteine and was less for all other compounds. Total 75Se excretion in the urine was highest from rats given trimethylselenonium (about 90%, both doses) and was lowest from rats given selenomethionine (4%, low dose). Urine samples were chromatographed on SP-Sephadex cation-exchange columns and 75Se was eluted with ammonium formate; trimethylselenonium was precipitated with ammonium Reineckete solution and trimethylsulfonium carrier. Urinary trimethylselenonium excretion was greatest from rats given trimethylselenonium, but rats given Se-dimethylselenocysteineselenonium (low dose) excreted 35-45% of the dose as trimethylselenonium ion. The lowest quantity of trimethylselenonium was excreted by rats given the low dose of selenomethionine (0-3%). Pancreas, kidney, and liver showed the highest uptake (% of dose/g) of the selenium compounds. Trimethylselenonium was highly concentrated by the kidney and also showed high myocardial uptake (heart/blood ratio = 5) 0.5 h after injection; the selective uptake of trimethylselenonium in heart was not observed for the other selenonium compounds.

Animals↗
PubMed2006

Cancer chemoprevention: selenium as a prooxidant, not an antioxidant.

Although the average daily dietary selenium (Se) intake in the United States is consistently above the adult RDA of 55 microg Se/day, supranutritional supplements of 200 microg Se/day have been shown to provide chemopreventive benefits against several cancers, particularly prostate cancer. The hypothesis herein contends that selenium compounds with the greatest anticarcinogenic potency are likely to be sodium selenite with Se in the +4 oxidation state and methylseleninic acid. These compounds exert their cancer chemopreventive effects by directly oxidizing critical thiol-containing cellular substrates, and are more effective than the more frequently preferred (used) supplements of selenomethionine and Se-methylselenocysteine that lack oxidation capability. Selenate (+6 Se) the immediate precursor of selenite (+4 Se) can be metabolically reduced, and although less potent than the +4 Se compounds cited above, appears to be a more effective anticarcinogen than organic forms of dietary selenium. Apoptosis, an important, Se-induced anticarcinogenic mechanism, is accomplished by the direct oxidation of vicinal sulfhydryl groups in cysteine clusters within the catalytic domains of cellular enzymes (e.g., protein kinase C), and by the production of CH3Se-, which reacts with O2 to generate superoxide and other reactive oxygen species (ROS). Activated oncogenes "prime" cells for Se-induced prooxidative apoptosis thereby providing the needed margin for "killing" cancer cells while leaving normal, healthy cells unharmed. Selenoethers, such as selenomethionine and Se-methylselenocysteine are not oxidizing agents, and first, must be converted to methylselenol (CH3Se-) that can be directly oxidized to methylseleninic acid. The addition of methioninase, to selenomethionine, or beta-lyase to Se-methylselenocysteine, rapidly produces significant amounts of methylselenol, which may be oxidized to methylseleninic acid or may react with O2 to produce superoxide and ROS, resulting in anticarcinogenic activities comparable to selenite or methylseleninic acid. The relatively large amounts of selenomethionine or Se-methylselenocysteine needed to produce apoptosis in cancer cells compared with selenite or methylseleninic acid are a probable consequence of low tissue levels of the required enzymes. Even though many studies have consistently shown that selenomethionine is an ineffective anticarcinogen at doses corresponding to those currently allowed by the FDA, it has been chosen as the Se intervention agent in the 32,500-man (phase III), NCI-funded SELECT trial, which tests the effectiveness of dietary supplements of dietary supplements of Se and tocopherol, individually or in combination, in the prevention of prostate cancer. In 2013, when the data are in, the value of using Se supplements for cancer chemoprevention is likely to be underestimated.

Animals↗